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Related Concept Videos

Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Ligand-gated Ion Channels01:19

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Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

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Related Experiment Video

Updated: Jun 8, 2026

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
09:59

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices

Published on: July 17, 2011

Channel-mediated tonic GABA release from glia.

Soojung Lee1, Bo-Eun Yoon, Ken Berglund

  • 1Center for Neural Science, Korea Institute of Science and Technology (KIST), Seoul, Korea.

Science (New York, N.Y.)
|October 9, 2010
PubMed
Summary

Glial cells release the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) through the Bestrophin 1 (Best1) channel, mediating tonic inhibition in the cerebellum. This discovery reveals a novel mechanism for glial-neuronal communication in synaptic inhibition.

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Last Updated: Jun 8, 2026

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
09:59

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Published on: July 17, 2011

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices
07:32

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices

Published on: October 12, 2017

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
07:51

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors

Published on: November 14, 2014

Area of Science:

  • Neuroscience
  • Cell Biology
  • Neurochemistry

Background:

  • Synaptic inhibition relies on both tonic and phasic release of gamma-aminobutyric acid (GABA).
  • The precise mechanism governing tonic GABA release remains largely undetermined.
  • Phasic GABA release is understood to originate from Ca(2+)-dependent neuronal exocytosis.

Purpose of the Study:

  • To elucidate the molecular mechanism underlying tonic GABA release in the cerebellum.
  • To investigate the role of glial cells and specific ion channels in tonic inhibition.
  • To establish the contribution of glial-derived GABA to neuronal function.

Main Methods:

  • Utilized electrophysiological recordings to assess synaptic inhibition.
  • Employed genetic silencing techniques to investigate the role of Bestrophin 1 (Best1).
  • Performed selective Best1 expression in glial cells to rescue tonic inhibition.

Main Results:

  • Identified GABA permeation through the Bestrophin 1 (Best1) anion channel as the source of tonic GABA release from glial cells.
  • Demonstrated that silencing Best1 completely eliminates tonic inhibition in the cerebellum.
  • Showcased that selective re-expression of Best1 in glial cells fully restores tonic inhibition.

Conclusions:

  • Established Bestrophin 1 (Best1) as the key molecular player mediating tonic GABA release from glial cells.
  • Identified a novel pathway for glial-neuronal communication in regulating synaptic inhibition.
  • Highlighted the critical role of glial cells in tonic inhibition through Best1-mediated GABA permeation.